ReviewFrontiers in molecular neuroscience2014
Emerging modes of PINK1 signaling: another task for MARK2.
Review in Frontiers in molecular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Role of MARK2 in the nervous system and cancer.Cancer gene therapy · 2024Review
- Tactics with Prebiotics for the Treatment of Metabolic Dysfunction-Associated Fatty Liver Disease via the Improvement of Mitophagy.International journal of molecular sciences · 2023Review
- Validating MARK2 Gene Polymorphism as a Predictor of Response to Lithium Treatment in Bipolar PatientsIranian biomedical journal · 2022Article
- Memantine Improves Cognitive Function and Alters Hippocampal and Cortical Proteome in Triple Transgenic Mouse Model of Alzheimer's Disease.Experimental neurobiology · 2019Article
- Back to the tubule: microtubule dynamics in Parkinson's disease.Cellular and molecular life sciences : CMLS · 2017Review
- Epigenetic Treatment of Neurodegenerative Ophthalmic Disorders: An Eye Toward the Future.BioResearch open access · 2017Review
- MARK2 Rescues Nogo-66-Induced Inhibition of Neurite Outgrowth via Regulating Microtubule-Associated Proteins in Neurons In Vitro.Neurochemical research · 2016Article
- PINK1 kinase catalytic activity is regulated by phosphorylation on serines 228 and 402.The Journal of biological chemistry · 2015Article
- Regulation and targeting of enzymes mediating Parkinson's disease pathogenesis: focus on Parkinson's disease kinases, GTPases, and ATPases.Frontiers in molecular neuroscience · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PTEN-induced kinase 1 (PINK1) acts at multiple levels to promote mitochondrial health, including regulatory influence on ATP-synthesis, protein quality control, apoptosis, mitochondrial transport, and destiny. PINK1 mutations are linked to Parkinson disease (PD) and mostly result in loss of kinase activity. But the molecular events responsible for neuronal death as well as the physiological targets and regulators of PINK1 are still a matter of debate. This review highlights the recent progress evolving the cellular functions of the cytosolic pool of PINK1 in mitochondrial trafficking and neuronal differentiation. Regulation of PINK1 signaling occurs by mitochondrial processing to truncated forms of PINK1, differentially targeted to several subcellular compartments. The first identified activating kinase of PINK1 is MAP/microtubule affinity regulating kinase 2 (MARK2), which phosphorylates T313, a frequent mutation site linked to PD. Kinases of the MARK2 family perform diverse functions in neuronal polarity, transport, migration, and neurodegeneration such as Alzheimer disease (AD). This new protein kinase signaling axis might provide a link between neurodegenerative processes in AD and PD diseases and opens novel possibilities in targeting pathological signaling processes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.